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Please find a new neurologist. Your husband's story sounds like APS. This has only been diagnosed for 20 years and so many doctors dont understand the issues. The APS tests fluctuate.... you must take the test every 6-12 weeks a few times to really rule out APS. Sometimes the IgG will be low or normal or high.... throughout your life. The clinical and MRI reports are often identical to multiple sclerosis. Your husband is worth the money to fly to a true Multiple Sclerosis Neurologist. Also demand a EVP test and visit an Eye specialist. They can really see the brain lesions and check him for Wilsons disease....another MS mimic.... It is also possible to have more than one disease; our bodies are wonderful but imperfect.... Research your doctors, request in writting your husbands medical reports... you have the right and they are free or low cost to you..... and study each page. Doctors are not any smarter than the average bear....they just went to school.

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I'm not sure anyone on here really even cares about this anymore, but I finally put together the remaining of puzzle piece regarding Jeff's first flare, his strange blood numbers and hypercoagulation, and just wanted to document it here on the hypercoagulation thread. This was the reason I started looking into vascular issues in the first place. And now I'm done.
http://ajp.amjpathol.org/cgi/reprint/169/2/566.pdf

Hypoxia is a critical factor for cell death or survival in ischemic stroke, but the pathological consequences of combined ischemia-hypoxia are not fully understood. Here we examine this issue using a modifiedLevine/Vannucci procedure in adult mice that consists of unilateral common carotid artery occlusion and hypoxia with tightly regulated body temperature. At the cellular level , ischemia-hypoxia produced proinflammatory cytokines and simultaneously acti- vated both prosurvival (eg , synthesis of heat shock 70 protein , phosphorylation of ERK and AKT) and pro-apoptosis signaling pathways.

At the tissue level, ischemia-hypoxia caused persistent cerebral perfusion deficits even after release of the carotid artery occlusion. These changes were associated with both platelet deposition and fibrin accumulation within the cerebral circulation and would be expected to contribute to infarction. Complementary studies in fibrinogen-deficient mice revealed that the absence of fibrin and/or secondary fibrin-mediated inflammatory processes significantly attenuated brain damage. Together, these results suggest that ischemia-hypoxia is a powerful stimulus forspontaneous coagulation leading to reperfusion deficits and autophagic/lysosomal cell death in brain.

Dr. Mark Haacke and I have been communicating about this theory of an hypoxic event created by CCSVI and endothelial disruption initiating an MS flare. (see Lassmann studies on early MS lesions and hypoxia) He is following up on this theory in his new CCSVI testing protocol, and is already finding some interesting results, as MS patients show "stroke-like" cerebral damage, created by slowed perfusion. From his site:

Three interesting papers (13-15) point toward other features associated with venous congestion, small thrombi and iron deposition. In the first two, children with early cerebral infarction (13) and children following severe ischemic-anoxic events (14) showed increases in iron content in the basal ganglia, thalami and white matter. Iron deposition was also associated with periventricular gliosis (14). In fact, desferrioximine, an iron chelator, has been used to minimize the damage for patients undergoing cardiac resuscitation (16). These findings also may be consistent with the fact that some MS lesions show iron build up. It has not been shown yet but one might conjecture if the MS lesions with the highest iron content may represent ischemic tissue of lesions and may correspond with the lowest blood volume. Finally, an interesting case of venous congestion shown with SWI that was similar in appearance to a developmental venous anomaly, also in a child, shows that SWI may be able to detect small thrombosed veins. In this particular case, the child was treated and recovered and evidence of the problem on imaging disappeared at two months (15). So iron regulation appears to be disrupted in ischemic-anoxic insult. Could this be what is happening in MS as well? (13) Cross et al (1990). MR evaluation of brain iron in children with cerebral infarction. AJNR 11; 341-348.(14) Dietrich et al (1988). Iron accumulation in the basal ganglia following severe ischemic-anoxic insults in children. Radiology 168; 203-206.(15) Amemiya et al (2008). Venous congestion associated with developmental venous anomaly: Findings on susceptibility weighted imaging. JMRI 28: 1506-1509. (16) Gutteridge et al (1979). Inhibition of the iron-catalysed formation of hydroxyl radicals from superoxide and of lipid peroxidation by desferrioxamine. Biochem J 184; 469-472.

CCSVI + endothelial disruption= an hypoxic event initiating coagulation cascade and cerebral infarction, leading to iron deposition in brain tissue, activating immune system response. MS in theory. Time and research will tell the rest.

Excellent post, Cheer. As ever!
I still have lots of fibrin-munching supplements like lumbrokinase and serrapeptase though I haven't wanted to take any since the operation. I do remember that when I took them for a while back in 07 or 08 that I felt modestly better.

gibbledygook wrote:Excellent post, Cheer. As ever!I still have lots of fibrin-munching supplements like lumbrokinase and serrapeptase though I haven't wanted to take any since the operation. I do remember that when I took them for a while back in 07 or 08 that I felt modestly better.

Thanks, dear Gibbs.

I think fibrin munching, proteolytic enzymes and the like are a smart thing to continue for general health. Tough to know what supps are OK to take during pregnancy. Maybe consult your ob gyn? We're having a good discussion about this on the CCSVI thread- continuing on from a Dom oldie but goody post.
http://www.thisisms.com/ftopict-8277.htmlbe well,
cheer

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